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Diabetic ketoacidosis in a patient with chronic calcific pancreatitis after minor papilla stent insertion
D Bhasin, R Sidhu, A Bhansali, et al.
Chronic calcific pancreatitis: diabetic ketoacidosis after stent insertion
2. Wolkenstein P, Revuz J. Drug induced severe skin reactionsincidence, management and prevention. Drug Saf 1995;13: 56-68. 3. Womack CR, Randall CC. Erythema exudative multiforme: its association with viral infections. Am J Med 1953;15: 633-44. 4. Alexander MK, Cope S. Erythema multiforme exudativum (Stevens-Johnson syndrome). J Pathol Bacteriol 1954;68:373-80. 5. Heer M, Altorfer J, Burger HS, Walti M. Bullous esophageal lesions due to cotrimoxazole: an immune mediated process? Gastroenterology 1985;88:1954-7. 6. Zweiban B, Cohen H, Chandrasoma P. Gastrointestinal involvement complicating Stevens-Johnson syndrome. Gastroenterology 1986;91:469-74. 7. Peters ME, Gourley G, Mann FA. Esophageal stricture and web secondary to Stevens-Johnson syndrome. Pediatr Radiol 1983;13:290-1. 8. Howell CG, Mansberger JA, Parrish RA. Esophageal stricture secondary to Stevens-Johnson syndrome. J Pediatr Surg 1987;22:994-5. 9. Rottermann EM, Julia MV, Rovira J, Pari FJ, Morales L. Esophageal stenosis following Stevens-Johnson syndrome. Clin Pediatr (Phila) 1990;29:336-45. 10. Chabas E, Salazar F, Rovira I, Nalda MA. Sindrome de Stevens-Johnson associado a estenosis esofagica. Rev Esp Anestesiol Reanim 1990;37:364-5. 11. Edell DS, Davidson JJ, Muelenaer AA, Majure M. Unusual manifestation of Stevens-Johnson syndrome involving the respiratory and gastrointestinal tract. Pediatrics 1992;89:429-32.
12. Stein MR, Thompson CK, Sawicki JE, Martel AJ. Esophageal stricture complicating Stevens-Johnson syndrome. Am J Gastroenterol 1974;62:435-9. 13. Tan Y, Goh K. Esophageal stricture as a late complication of Stevens-Johnson syndrome. Gastrointest Endosc 1999;50:566-8. 14. Schopf E, Stuhmer A, Rzany B, Victor N, Zentgraf R, Kapp JF. Toxic epidermal necrosis and Stevens-Johnson syndrome: an epidemiological study from West Germany. Arch Dermatol 1991;127:839-42. 15. Batusji-Garins S, Rzany B, Stern RS, Shear NH, Naldi L, Roujeau JC. Clinical classification of cases of epidermal necrolysis, Stevens-Johnson syndrome and erythema multiforme. Arch Dermatol 1993;129:92-6. 16. Becker DS. Toxic epidermal necrolysis. Lancet 1998;351: 1417-20. 17. Rzany B, Mockenhaupt M, Baur S, Schroder W, Stocker U, Mueller J, et al. Epidemiology of erythema exsudativum multiforme majus, Stevens-Johnson syndrome, and toxic epidermal necrolysis in Germany (1990-1992): structure and results of a population-based registry. J Clin Epidemiol 1996;49:769-73. 18. Sontheimer RD, Garibaldi RA, Krueger CG. Stevens-Johnson syndrome associated with Mycoplasma pneumoniae infection. Arch Dermatol 1978;114:241-4. 19. Wooten JW, Katz HI, Hoffman S, Link JF. Development of oral lesions in erythema multiforme exudativum. Oral Surg Oral Med Oral Pathol 1967;24:808-16. 20. Katzka DA. Caustic injury to the upper gastrointestinal tract. In: Brandt L, editor. Clinical practice of gastroenterology. Philadelphia: Current Medicine; 1999. p. 96-104. p. 808-16.
Diabetic ketoacidosis in a patient with chronic calcific pancreatitis after minor papilla stent insertion
ketoacidosis within 3 months of stent insertion via the minor papilla for chronic intractable pain.
Deepak Kumar Bhasin, MD, DM, Rupinder Singh Sidhu, MD, Anil Bhansali, MD, DM, Birinder Nagi, MD
A 56-year-old man was hospitalized with complaints of epigastric pain, diarrhea, and significant weight loss of 2 months’ duration. Chronic calcific pancreatitis was diagnosed 7 years earlier based on typical pancreatic pain and the presence of pancreatic calcification on an abdominal radiograph. The patient continued to drink alcohol (100 g/d), which he had done for 10 years and frequently took analgesic medication for relief of pain. Diabetes mellitus was diagnosed 2 years earlier, and blood glucose levels had been controlled by orally administered glibenclamide. The severity of the pain had increased over the prior 2 months, and, in addition to diarrhea, the patient passed oil droplets. He had lost about 20 kg of weight over several months despite a well-preserved appetite. He smoked 10 cigarettes per day for the last 15 years. On examination, there was evidence of malnutrition (body mass index 18.75 kg/m2), pallor, and bilateral pitting pedal edema. Pulse rate was 88 per minute and blood pressure was 110/70 mm Hg. The abdomen was normal except for mild epigastric tenderness. Systemic examination was otherwise unremarkable. The Hb level was 11.1 g/dL (normal: 12-18 g/dL), and total and differential leukocyte counts were normal. Biochemical tests of liver function were within normal ranges. Serum amylase was 160 IU/L (72-160 IU/L). Urinanalysis revealed glycosuria. Fasting and post-prandial blood
Chronic pancreatitis is characterized by irreversible destruction and fibrosis of pancreatic parenchyma, ultimately leading to exocrine and endocrine deficiency. Although patients with chronic pancreatitis are particularly prone to hypoglycemia, ketoacidosis is distinctly uncommon, even if insulin treatment is withdrawn.1-3 However, ketoacidosis can occur during stress and after correction of maldigestion by administration of potent pancreatic enzyme supplements.4 A case is reported of pancreas divisum, alcohol-induced chronic calcific pancreatitis and diabetes, in which the presentation was diabetic Current affiliations: Department of Gastroenterology, Department of Endocrinology, Department of Gastrointestinal Radiology, Post Gradute Institute of Medical Education and Research, Chandigarh, India. Reprint requests: Dr. Deepak Kumar Bhasin, #1041, Sector 24-B, Chandigarh, 160 023, India. Copyright Ó 2004 by the American Society for Gastrointestinal Endoscopy 0016-5107/$30.00 PII: S0016-5107(03)02821-9 440
GASTROINTESTINAL ENDOSCOPY
CASE REPORT
VOLUME 59, NO. 3, 2004
Chronic calcific pancreatitis: diabetic ketoacidosis after stent insertion
Figure 1. CT, showing multiple hyperdense foci in pancreas and dilated pancreatic duct.
Figure 2. Radiograph, showing guidewire in dorsal pancreatic duct after contrast-free cannulation of minor papilla.
glucose levels were, respectively, 235 mg/dL (70-105 mg/ dL) and 435 mg/dL (140-200 mg/dL). A D-xylose test was normal; a quantitative fecal fat determination was 14.75 g/ d (6 g/d). A plain radiograph of the abdomen disclosed calcification diffusely throughout the pancreas. Contrastenhanced CT demonstrated dilatation of the main pancreatic duct, with ductal and parenchymal calcifications (Fig. 1) but no evidence of necrosis, pseudocyst, or pseudoaneurysm. Varices were not found on upper endoscopy. Multiple subcutaneous injections of up to 48 units of insulin were VOLUME 59, NO. 3, 2004
D Bhasin, R Sidhu, A Bhansali, et al.
Figure 3. Retrograde pancreatogram made via minor papilla, showing dilated dorsal duct with multiple filling defects caused by calculi and dilated dorsal duct branches also with multiple filing defects. Bile duct (arrow) is also opacified.
Figure 4. Retrograde pancreatogram, showing 7F stent in dorsal pancreatic duct. required to control blood glucose levels. Steatorrhea improved with substitution of medium chain triglycerides for dietary fat and pancreatic enzyme supplementation. Endoscopic cannulation of the major and minor papilla followed by retrograde injection of contrast medium revealed pancreas divisum (Fig. 2). The dorsal pancreatic duct was dilated and contained stones (Fig. 3). A 7F stent was placed across the minor papilla (Fig. 4). Pancreatic enzyme supplements were stopped to study the effect of stent placement on pancreatic exocrine function, and the patient was advised to stop drinking alcohol. Over the next GASTROINTESTINAL ENDOSCOPY
441
D Bhasin, R Sidhu, A Bhansali, et al.
Chronic calcific pancreatitis: diabetic ketoacidosis after stent insertion
3 months, there was marked improvement in the pain and steatorrhea, and the patient gained 5 kg of weight. A fecal fat determination was 9 g/d. However, control of the diabetes worsened and treatment with metformin was started in addition to insulin. Three months later, the patient presented with altered sensorium, and a diagnosis of diabetic ketoacidosis was made. Blood glucose was 471 mg/dL, pH 6.94 (7.34-7.44), bicarbonate level 03 mEq/L (18-28 mEq/L) and PCO2 13 mm Hg (40 mm Hg). The urine was strongly positive for ketones. The total leukocyte count was 2.9 3 103/lL (4-11 3 103/ lL) with 92% neutrophils (40%-75%) and 8% lymphocytes (20%-45%). The blood urea was 95 mg/dL (20-40 mg/dL), and serum creatinine was 2.3 mg/dL (0.6-1.2 mg/dL). Serum electrolytes were within normal limits. The patient was treated with insulin infusion; sodium bicarbonate was infused to correct the acidosis. Sensorium and renal functions improved. Oral feeding was resumed on the 4th hospital day. Treatment at discharge included insulin injections. Fasting C-peptide level was less than 0.50 ng/ mL (0.9-4.0 ng/mL) and fasting glucagon was 30 pg/mL (20100 pg/mL). On follow-up, the patient was asymptomatic, and blood glucose levels were controlled with insulin injections and orally administered metformin.
DISCUSSION Exocrine and endocrine dysfunction, inevitable consequences of chronic pancreatitis, occur long term in the majority of patients.1 Patients with chronic pancreatitis are resistant to ketosis for various reasons: relative preservation of islet cell function as compared with patients with type-1 diabetes mellitus; reduced secretion of glucagon, an important ketogenic stimulus; lower adipose tissue stores of triglyceride, which acts as a substrate for ketogenesis; and impairment of hepatic ketogenesis, which also may contribute to resistance to ketosis. Our patient had chronic calcific pancreatitis and pancreas divisum, with dorsal duct changes of chronic pancreatitis (dilation of main duct and side branches, and ductal calculi). The majority of patients with pancreas divisum are asymptomatic. However, this anomaly may be associated with acute recurrent pancreatitis, chronic pancreatitis, and rarely with other known causes of chronic pancreatitis, such as excessive alcohol ingestion and tropical pancreatitis.6-10 It is likely that our patient developed chronic calcific pancreatitis as a result of alcohol ingestion, with a contribution from the pancreas divisum. Of patients with pancreas divisum, those with acute recurrent pain respond best to pancreatic duct decompression compared with patients with chronic pancreatitis.6-8 However, placement of a 7F stent at the minor papilla led to dramatic relief of pain in our patient, which seems inconsistent with the response to discontinuation of alcohol consumption 442
GASTROINTESTINAL ENDOSCOPY
alone. Increasing doses of insulin were required after pancreatic stent placement. Data on the effects of pancreatic duct decompression on exocrine and endocrine functions in patients of chronic pancreatitis are conflicting, with evidence that pancreatic function may improve,11-13 remain unchanged,14,15 or even worsen.16 Although treatment with pancreatic enzyme supplements can relieve pain and correct maldigestion, it also can cause potentially life-threatening disturbances in glucose control for patients with chronic pancreatitis who are taking insulin. O’Keefe et al.4 studied the effect of potent pancreatic enzyme supplements in patients with chronic pancreatitis, a significant number of whom were taking insulin for control of diabetes. In this study, blood glucose levels were abnormal in the majority of the patients after treatment with potent pancreatic enzymes; one patient developed diabetic ketoacidosis. Analogous to these findings, our patient developed ketosis within 3 months of minor papilla stent insertion in the absence of any precipitating factor and while taking adequate doses of insulin. C-peptide levels were low, indicting low insulin secretion, and glucagon levels were within normal limits. Stent insertion resulted in significant pain relief, improvement in appetite and steatorrhea, and a weight gain of 5 kg. It is our belief that, in the presence of preserved glucagon secretion, correction of maldigestion and the resultant increase in fat stores after stent insertion may have resulted in the development of ketoacidosis. This observation underscores the importance of careful control of glucose levels in malnourished diabetic patients after pancreatic stent insertion. REFERENCES 1. Ammann RW, Buehler H, Freiburghaus AW, Siegenthaler W. Differences in the natural history of idiopathic (nonalcoholic) and alcoholic chronic pancreatitis. A comparative long-term study of 287 patients. Pancreas 1987;2:368-77. 2. Bank S, Marks IN, Vinik AI. Clinical and hormonal aspects of pancreatic diabetes. Am J Gastroenterol 1975;64:13-22. 3. Kalk WJ, Vinik AI, Bank S. Insulin secretion and exocrine function in patients with chronic pancreatitis. Diabetologia 1979;16:355-8. 4. O’Keefe SJ, Cariem AK, Levy M. The exacerbation of pancreatic endocrine dysfunction by potent pancreatic exocrine supplements in patients with chronic pancreatitis. J Clin Gastroenterol 2001;32:319-23. 5. Malchoff CD, Pohl SL, Kaiser DL, Carey RM. Determinants of glucose and ketoacid concentrations in acutely hyperglycemic patients. Am J Med 1984;77:275-85. 6. Cotton PB. Congenital anomaly of pancreas divisum as a cause of obstructive pain and pancreatitis. Gut 1980;21:105-7. 7. Delhaye M, Engelholm L, Cremer M. Pancreas divisum: congenital anatomic variant or anomaly? Gastroenterology 1985;89:1431-5. VOLUME 59, NO. 3, 2004
EMR of ileal adenoma
K Tsuchida, N Okayama, Y Yokoyama, et al.
8. Bhasin DK, Poddar U. Endoscopic management of chronic pancreatitis. In: Bhutani MS, Tandon RK, editors. Advances in gastrointestinal endoscopy. 1st ed. New Delhi: Jaypee Brothers Medical Publishers; 2001. p. 284-302. 9. Bhasin DK, Sriram PVJ, Nagi B, Varma V, Singh K. Endoscopic stenting of minor papilla for symptomatic pancreatic divisum. Indian J Gastroenterol 1997;16:30-1. 10. Bhasin DK, Dhavan S, Sriram PVJ, Nagi B, Varma V, Singh G, et al. Endoscopic management of pancreatic diseases. Indian J Gastroenterol 1997;16:151-2. 11. Buchler M, Friess H, Bittner R, Roscher R, Krautzberger W, Muller M, et al. Duodenum preserving pancreatic head resection: Long-term results. J Gastrointest Surg 1997;1:13-7. 12. Nealon WH, Thompson JC. Progressive loss of pancreatic function in chronic pancreatitis is delayed by main duct decompression. Ann Surg 1993;217:458-68.
13. Sidhu SS, Nundy S, Tandon RK. The effect of the modified Puestow procedure on diabetes in patients with tropical chronic pancreatitis: a positive study. Am J Gastroenterol 2001;96:107-11. 14. Sato T, Miyashita E, Yamauchi H, Matsuno S. The role of surgical treatment for chronic pancreatitis. Ann Surg 1986; 203:266-71. 15. Adamek HE, Jakobs R, Buttmann A, Adamek MU, Schneider ARJ, Riemann JF. Long term follow up of patients with chronic pancreatitis and pancreatic stones treated with extracorporeal shock wave lithotripsy. Gut 1999;45:402-6. 16. Ammann RW, Akovbiantz A, Largiader F, Scheueler G. Course and outcome of chronic pancreatitis. Longitudinal study of a mixed medical-surgical series of 245 patients. Gastroenterology 1984;86:820-7.
EMR of ileal adenoma: report of two cases Kenji Tsuchida, MD, Naotsuka Okayama, MD, Yoshifumi Yokoyama, MD, Takashi Joh, MD, Kyoji Seno, MD, Hirotaka Ohara, MD, Makoto Sasaki, MD, Hiromi Kataoka, MD, Fuminori Okumura, MD, Makoto Itoh, MD
Various types of malignant tumor, such as lymphoma and carcinoma, arise in the terminal ileum,1 but adenoma is rare in this segment of the small intestine. Two cases are reported in which an adenoma in the terminal ileum was removed by EMR. Endoscopic and stereomicroscopic findings are presented. The clinical benefit of EMR for ileal adenoma is discussed. CASE REPORT Case 1 A 65-year-old man presented with hematochezia. There was a history of laparotomy 24 years earlier for duodenal ulcer. The family history was unremarkable. At a prior colonoscopy, 5 colonic polyps and one ileal polyp were found, and the patient was referred for further evaluation and treatment. The abdomen was soft and flat, a surgical scar was present, and there was no tenderness or palpable mass. Laboratory data included an alkaline phosphatase of 274 U/L (normal: 60-230 U/L) and carcinoembryonic antigen level of 9.3 ng/mL (<5 ng/mL). Colonoscopy revealed a slightly white, flat-elevated 7mm tumor with a central depression and slightly irregular Current affiliations: Internal Medicine, Nagoya City Johsai Hospital, Nagoya City University Graduate School of Medical Sciences, Department of Internal Medicine and Bioregulation, Nagoya, Japan. Reprint requests: Kenji Tsuchida, MD, PhD, Internal Medicine, Nagoya City Johsai Hospital, 4-1 Kitabata-cho, Nakamura-ku, Nagoya 453-0815, Japan. Copyright Ó 2004 by the American Society for Gastrointestinal Endoscopy 0016-5107/$30.00 PII: S0016-5107(03)02820-7 VOLUME 59, NO. 3, 2004
Figure 1. A, Endoscopic view, showing ileal adenoma (Case 1). B, Chromoendoscopic view of ileal adenoma. surface in the ileum 8 cm from the ileocecal valve (Fig. 1A). Chromoscopy (0.08% indigo carmine) demonstrated irregularity of the tumor surface (Fig. 1B). There seemed to be no invasion into the submucosal layer, because probing with a forceps disclosed that the lesion was mobile. Biopsy specimens revealed the tumor to be an adenoma. Barium GASTROINTESTINAL ENDOSCOPY
443
Chronic calcific pancreatitis: diabetic ketoacidosis after stent insertion
2. Wolkenstein P, Revuz J. Drug induced severe skin reactionsincidence, management and prevention. Drug Saf 1995;13: 56-68. 3. Womack CR, Randall CC. Erythema exudative multiforme: its association with viral infections. Am J Med 1953;15: 633-44. 4. Alexander MK, Cope S. Erythema multiforme exudativum (Stevens-Johnson syndrome). J Pathol Bacteriol 1954;68:373-80. 5. Heer M, Altorfer J, Burger HS, Walti M. Bullous esophageal lesions due to cotrimoxazole: an immune mediated process? Gastroenterology 1985;88:1954-7. 6. Zweiban B, Cohen H, Chandrasoma P. Gastrointestinal involvement complicating Stevens-Johnson syndrome. Gastroenterology 1986;91:469-74. 7. Peters ME, Gourley G, Mann FA. Esophageal stricture and web secondary to Stevens-Johnson syndrome. Pediatr Radiol 1983;13:290-1. 8. Howell CG, Mansberger JA, Parrish RA. Esophageal stricture secondary to Stevens-Johnson syndrome. J Pediatr Surg 1987;22:994-5. 9. Rottermann EM, Julia MV, Rovira J, Pari FJ, Morales L. Esophageal stenosis following Stevens-Johnson syndrome. Clin Pediatr (Phila) 1990;29:336-45. 10. Chabas E, Salazar F, Rovira I, Nalda MA. Sindrome de Stevens-Johnson associado a estenosis esofagica. Rev Esp Anestesiol Reanim 1990;37:364-5. 11. Edell DS, Davidson JJ, Muelenaer AA, Majure M. Unusual manifestation of Stevens-Johnson syndrome involving the respiratory and gastrointestinal tract. Pediatrics 1992;89:429-32.
12. Stein MR, Thompson CK, Sawicki JE, Martel AJ. Esophageal stricture complicating Stevens-Johnson syndrome. Am J Gastroenterol 1974;62:435-9. 13. Tan Y, Goh K. Esophageal stricture as a late complication of Stevens-Johnson syndrome. Gastrointest Endosc 1999;50:566-8. 14. Schopf E, Stuhmer A, Rzany B, Victor N, Zentgraf R, Kapp JF. Toxic epidermal necrosis and Stevens-Johnson syndrome: an epidemiological study from West Germany. Arch Dermatol 1991;127:839-42. 15. Batusji-Garins S, Rzany B, Stern RS, Shear NH, Naldi L, Roujeau JC. Clinical classification of cases of epidermal necrolysis, Stevens-Johnson syndrome and erythema multiforme. Arch Dermatol 1993;129:92-6. 16. Becker DS. Toxic epidermal necrolysis. Lancet 1998;351: 1417-20. 17. Rzany B, Mockenhaupt M, Baur S, Schroder W, Stocker U, Mueller J, et al. Epidemiology of erythema exsudativum multiforme majus, Stevens-Johnson syndrome, and toxic epidermal necrolysis in Germany (1990-1992): structure and results of a population-based registry. J Clin Epidemiol 1996;49:769-73. 18. Sontheimer RD, Garibaldi RA, Krueger CG. Stevens-Johnson syndrome associated with Mycoplasma pneumoniae infection. Arch Dermatol 1978;114:241-4. 19. Wooten JW, Katz HI, Hoffman S, Link JF. Development of oral lesions in erythema multiforme exudativum. Oral Surg Oral Med Oral Pathol 1967;24:808-16. 20. Katzka DA. Caustic injury to the upper gastrointestinal tract. In: Brandt L, editor. Clinical practice of gastroenterology. Philadelphia: Current Medicine; 1999. p. 96-104. p. 808-16.
Diabetic ketoacidosis in a patient with chronic calcific pancreatitis after minor papilla stent insertion
ketoacidosis within 3 months of stent insertion via the minor papilla for chronic intractable pain.
Deepak Kumar Bhasin, MD, DM, Rupinder Singh Sidhu, MD, Anil Bhansali, MD, DM, Birinder Nagi, MD
A 56-year-old man was hospitalized with complaints of epigastric pain, diarrhea, and significant weight loss of 2 months’ duration. Chronic calcific pancreatitis was diagnosed 7 years earlier based on typical pancreatic pain and the presence of pancreatic calcification on an abdominal radiograph. The patient continued to drink alcohol (100 g/d), which he had done for 10 years and frequently took analgesic medication for relief of pain. Diabetes mellitus was diagnosed 2 years earlier, and blood glucose levels had been controlled by orally administered glibenclamide. The severity of the pain had increased over the prior 2 months, and, in addition to diarrhea, the patient passed oil droplets. He had lost about 20 kg of weight over several months despite a well-preserved appetite. He smoked 10 cigarettes per day for the last 15 years. On examination, there was evidence of malnutrition (body mass index 18.75 kg/m2), pallor, and bilateral pitting pedal edema. Pulse rate was 88 per minute and blood pressure was 110/70 mm Hg. The abdomen was normal except for mild epigastric tenderness. Systemic examination was otherwise unremarkable. The Hb level was 11.1 g/dL (normal: 12-18 g/dL), and total and differential leukocyte counts were normal. Biochemical tests of liver function were within normal ranges. Serum amylase was 160 IU/L (72-160 IU/L). Urinanalysis revealed glycosuria. Fasting and post-prandial blood
Chronic pancreatitis is characterized by irreversible destruction and fibrosis of pancreatic parenchyma, ultimately leading to exocrine and endocrine deficiency. Although patients with chronic pancreatitis are particularly prone to hypoglycemia, ketoacidosis is distinctly uncommon, even if insulin treatment is withdrawn.1-3 However, ketoacidosis can occur during stress and after correction of maldigestion by administration of potent pancreatic enzyme supplements.4 A case is reported of pancreas divisum, alcohol-induced chronic calcific pancreatitis and diabetes, in which the presentation was diabetic Current affiliations: Department of Gastroenterology, Department of Endocrinology, Department of Gastrointestinal Radiology, Post Gradute Institute of Medical Education and Research, Chandigarh, India. Reprint requests: Dr. Deepak Kumar Bhasin, #1041, Sector 24-B, Chandigarh, 160 023, India. Copyright Ó 2004 by the American Society for Gastrointestinal Endoscopy 0016-5107/$30.00 PII: S0016-5107(03)02821-9 440
GASTROINTESTINAL ENDOSCOPY
CASE REPORT
VOLUME 59, NO. 3, 2004
Chronic calcific pancreatitis: diabetic ketoacidosis after stent insertion
Figure 1. CT, showing multiple hyperdense foci in pancreas and dilated pancreatic duct.
Figure 2. Radiograph, showing guidewire in dorsal pancreatic duct after contrast-free cannulation of minor papilla.
glucose levels were, respectively, 235 mg/dL (70-105 mg/ dL) and 435 mg/dL (140-200 mg/dL). A D-xylose test was normal; a quantitative fecal fat determination was 14.75 g/ d (6 g/d). A plain radiograph of the abdomen disclosed calcification diffusely throughout the pancreas. Contrastenhanced CT demonstrated dilatation of the main pancreatic duct, with ductal and parenchymal calcifications (Fig. 1) but no evidence of necrosis, pseudocyst, or pseudoaneurysm. Varices were not found on upper endoscopy. Multiple subcutaneous injections of up to 48 units of insulin were VOLUME 59, NO. 3, 2004
D Bhasin, R Sidhu, A Bhansali, et al.
Figure 3. Retrograde pancreatogram made via minor papilla, showing dilated dorsal duct with multiple filling defects caused by calculi and dilated dorsal duct branches also with multiple filing defects. Bile duct (arrow) is also opacified.
Figure 4. Retrograde pancreatogram, showing 7F stent in dorsal pancreatic duct. required to control blood glucose levels. Steatorrhea improved with substitution of medium chain triglycerides for dietary fat and pancreatic enzyme supplementation. Endoscopic cannulation of the major and minor papilla followed by retrograde injection of contrast medium revealed pancreas divisum (Fig. 2). The dorsal pancreatic duct was dilated and contained stones (Fig. 3). A 7F stent was placed across the minor papilla (Fig. 4). Pancreatic enzyme supplements were stopped to study the effect of stent placement on pancreatic exocrine function, and the patient was advised to stop drinking alcohol. Over the next GASTROINTESTINAL ENDOSCOPY
441
D Bhasin, R Sidhu, A Bhansali, et al.
Chronic calcific pancreatitis: diabetic ketoacidosis after stent insertion
3 months, there was marked improvement in the pain and steatorrhea, and the patient gained 5 kg of weight. A fecal fat determination was 9 g/d. However, control of the diabetes worsened and treatment with metformin was started in addition to insulin. Three months later, the patient presented with altered sensorium, and a diagnosis of diabetic ketoacidosis was made. Blood glucose was 471 mg/dL, pH 6.94 (7.34-7.44), bicarbonate level 03 mEq/L (18-28 mEq/L) and PCO2 13 mm Hg (40 mm Hg). The urine was strongly positive for ketones. The total leukocyte count was 2.9 3 103/lL (4-11 3 103/ lL) with 92% neutrophils (40%-75%) and 8% lymphocytes (20%-45%). The blood urea was 95 mg/dL (20-40 mg/dL), and serum creatinine was 2.3 mg/dL (0.6-1.2 mg/dL). Serum electrolytes were within normal limits. The patient was treated with insulin infusion; sodium bicarbonate was infused to correct the acidosis. Sensorium and renal functions improved. Oral feeding was resumed on the 4th hospital day. Treatment at discharge included insulin injections. Fasting C-peptide level was less than 0.50 ng/ mL (0.9-4.0 ng/mL) and fasting glucagon was 30 pg/mL (20100 pg/mL). On follow-up, the patient was asymptomatic, and blood glucose levels were controlled with insulin injections and orally administered metformin.
DISCUSSION Exocrine and endocrine dysfunction, inevitable consequences of chronic pancreatitis, occur long term in the majority of patients.1 Patients with chronic pancreatitis are resistant to ketosis for various reasons: relative preservation of islet cell function as compared with patients with type-1 diabetes mellitus; reduced secretion of glucagon, an important ketogenic stimulus; lower adipose tissue stores of triglyceride, which acts as a substrate for ketogenesis; and impairment of hepatic ketogenesis, which also may contribute to resistance to ketosis. Our patient had chronic calcific pancreatitis and pancreas divisum, with dorsal duct changes of chronic pancreatitis (dilation of main duct and side branches, and ductal calculi). The majority of patients with pancreas divisum are asymptomatic. However, this anomaly may be associated with acute recurrent pancreatitis, chronic pancreatitis, and rarely with other known causes of chronic pancreatitis, such as excessive alcohol ingestion and tropical pancreatitis.6-10 It is likely that our patient developed chronic calcific pancreatitis as a result of alcohol ingestion, with a contribution from the pancreas divisum. Of patients with pancreas divisum, those with acute recurrent pain respond best to pancreatic duct decompression compared with patients with chronic pancreatitis.6-8 However, placement of a 7F stent at the minor papilla led to dramatic relief of pain in our patient, which seems inconsistent with the response to discontinuation of alcohol consumption 442
GASTROINTESTINAL ENDOSCOPY
alone. Increasing doses of insulin were required after pancreatic stent placement. Data on the effects of pancreatic duct decompression on exocrine and endocrine functions in patients of chronic pancreatitis are conflicting, with evidence that pancreatic function may improve,11-13 remain unchanged,14,15 or even worsen.16 Although treatment with pancreatic enzyme supplements can relieve pain and correct maldigestion, it also can cause potentially life-threatening disturbances in glucose control for patients with chronic pancreatitis who are taking insulin. O’Keefe et al.4 studied the effect of potent pancreatic enzyme supplements in patients with chronic pancreatitis, a significant number of whom were taking insulin for control of diabetes. In this study, blood glucose levels were abnormal in the majority of the patients after treatment with potent pancreatic enzymes; one patient developed diabetic ketoacidosis. Analogous to these findings, our patient developed ketosis within 3 months of minor papilla stent insertion in the absence of any precipitating factor and while taking adequate doses of insulin. C-peptide levels were low, indicting low insulin secretion, and glucagon levels were within normal limits. Stent insertion resulted in significant pain relief, improvement in appetite and steatorrhea, and a weight gain of 5 kg. It is our belief that, in the presence of preserved glucagon secretion, correction of maldigestion and the resultant increase in fat stores after stent insertion may have resulted in the development of ketoacidosis. This observation underscores the importance of careful control of glucose levels in malnourished diabetic patients after pancreatic stent insertion. REFERENCES 1. Ammann RW, Buehler H, Freiburghaus AW, Siegenthaler W. Differences in the natural history of idiopathic (nonalcoholic) and alcoholic chronic pancreatitis. A comparative long-term study of 287 patients. Pancreas 1987;2:368-77. 2. Bank S, Marks IN, Vinik AI. Clinical and hormonal aspects of pancreatic diabetes. Am J Gastroenterol 1975;64:13-22. 3. Kalk WJ, Vinik AI, Bank S. Insulin secretion and exocrine function in patients with chronic pancreatitis. Diabetologia 1979;16:355-8. 4. O’Keefe SJ, Cariem AK, Levy M. The exacerbation of pancreatic endocrine dysfunction by potent pancreatic exocrine supplements in patients with chronic pancreatitis. J Clin Gastroenterol 2001;32:319-23. 5. Malchoff CD, Pohl SL, Kaiser DL, Carey RM. Determinants of glucose and ketoacid concentrations in acutely hyperglycemic patients. Am J Med 1984;77:275-85. 6. Cotton PB. Congenital anomaly of pancreas divisum as a cause of obstructive pain and pancreatitis. Gut 1980;21:105-7. 7. Delhaye M, Engelholm L, Cremer M. Pancreas divisum: congenital anatomic variant or anomaly? Gastroenterology 1985;89:1431-5. VOLUME 59, NO. 3, 2004
EMR of ileal adenoma
K Tsuchida, N Okayama, Y Yokoyama, et al.
8. Bhasin DK, Poddar U. Endoscopic management of chronic pancreatitis. In: Bhutani MS, Tandon RK, editors. Advances in gastrointestinal endoscopy. 1st ed. New Delhi: Jaypee Brothers Medical Publishers; 2001. p. 284-302. 9. Bhasin DK, Sriram PVJ, Nagi B, Varma V, Singh K. Endoscopic stenting of minor papilla for symptomatic pancreatic divisum. Indian J Gastroenterol 1997;16:30-1. 10. Bhasin DK, Dhavan S, Sriram PVJ, Nagi B, Varma V, Singh G, et al. Endoscopic management of pancreatic diseases. Indian J Gastroenterol 1997;16:151-2. 11. Buchler M, Friess H, Bittner R, Roscher R, Krautzberger W, Muller M, et al. Duodenum preserving pancreatic head resection: Long-term results. J Gastrointest Surg 1997;1:13-7. 12. Nealon WH, Thompson JC. Progressive loss of pancreatic function in chronic pancreatitis is delayed by main duct decompression. Ann Surg 1993;217:458-68.
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EMR of ileal adenoma: report of two cases Kenji Tsuchida, MD, Naotsuka Okayama, MD, Yoshifumi Yokoyama, MD, Takashi Joh, MD, Kyoji Seno, MD, Hirotaka Ohara, MD, Makoto Sasaki, MD, Hiromi Kataoka, MD, Fuminori Okumura, MD, Makoto Itoh, MD
Various types of malignant tumor, such as lymphoma and carcinoma, arise in the terminal ileum,1 but adenoma is rare in this segment of the small intestine. Two cases are reported in which an adenoma in the terminal ileum was removed by EMR. Endoscopic and stereomicroscopic findings are presented. The clinical benefit of EMR for ileal adenoma is discussed. CASE REPORT Case 1 A 65-year-old man presented with hematochezia. There was a history of laparotomy 24 years earlier for duodenal ulcer. The family history was unremarkable. At a prior colonoscopy, 5 colonic polyps and one ileal polyp were found, and the patient was referred for further evaluation and treatment. The abdomen was soft and flat, a surgical scar was present, and there was no tenderness or palpable mass. Laboratory data included an alkaline phosphatase of 274 U/L (normal: 60-230 U/L) and carcinoembryonic antigen level of 9.3 ng/mL (<5 ng/mL). Colonoscopy revealed a slightly white, flat-elevated 7mm tumor with a central depression and slightly irregular Current affiliations: Internal Medicine, Nagoya City Johsai Hospital, Nagoya City University Graduate School of Medical Sciences, Department of Internal Medicine and Bioregulation, Nagoya, Japan. Reprint requests: Kenji Tsuchida, MD, PhD, Internal Medicine, Nagoya City Johsai Hospital, 4-1 Kitabata-cho, Nakamura-ku, Nagoya 453-0815, Japan. Copyright Ó 2004 by the American Society for Gastrointestinal Endoscopy 0016-5107/$30.00 PII: S0016-5107(03)02820-7 VOLUME 59, NO. 3, 2004
Figure 1. A, Endoscopic view, showing ileal adenoma (Case 1). B, Chromoendoscopic view of ileal adenoma. surface in the ileum 8 cm from the ileocecal valve (Fig. 1A). Chromoscopy (0.08% indigo carmine) demonstrated irregularity of the tumor surface (Fig. 1B). There seemed to be no invasion into the submucosal layer, because probing with a forceps disclosed that the lesion was mobile. Biopsy specimens revealed the tumor to be an adenoma. Barium GASTROINTESTINAL ENDOSCOPY
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